Fluid homeostasis after heart transplantation: the role of cardiac denervation.

摘要: Background : Orthotopic heart transplantation may interrupt key neural and humoral homeostatic mechanisms that normally adjust Na + fluid excretion to changes in intake. Such an interruption could lead plasma volume expansion. Methods We measured regulatory hormones under standardized conditions 11 transplant recipients (58 ± 7 years old ; mean standard deviation) 21 4 months after transplantation, 6 liver (51 old) 13 8 (cyclosporine control group), normal healthy subjects (61 9 old). Administration of all diuretics antihypertensive drugs was discontinued before the study. After 3 days during which ate a constant diet containing 87 mEq per 24 hours, by modified Evans blue dye (T-1824) dilution technique. Renal creatinine clearance blood samples were drawn for determination levels vasopressin, angiotensin II, aldosterone, atrial natriuretic peptide, renin activity. Results Supine resting activity, aldosterone (renin-angiotensin-aldosterone axis) vasopressin not different among control, transplant, groups. However, there trend toward elevated II (p ≤ 0.08) recipients. Atrial peptide significantly two threefold when compared with those Blood volume, normalized body weight (milliliters kilogram), greater (14%) subjects. values did differ ≥ 0.05) between Conclusions Extracellular expansion (+14%) occurs clinically stable who become hypertensive. Although hyperactivity renin-angiotensin-aldosterone axis is apparent supine conditions, our data suggest system responsive hypervolemic stimulus this likely consequence chronic cardiac deafferentation. Thus, poor adaptation retention be partly responsible incidence severity posttransplantation hypertension some